Prostate cancer is one of the major causes of death in men of the Western world. There are over 317,100 newly diagnosed cases and around 41,500 prostate cancer related deaths reported in North America (Kondo, et al., 2000). Of the people diagnosed for prostate cancer, approximately 20% of them will eventually develop androgen-independent tumors for which there is no effective cure (Voeks, et al., 2002).
As of now, treatment of non-organ confined prostatic carcinoma requires either surgical or pharmacological castration. While surgery and radiation therapy are also effective for treatment of localized tumors, there is no effective cure for advanced or metastatic tumors, tumors made up of cancerous cells which migrate from the original site to other sites in the body. Hormonal therapies and chemotherapy are also available but they are generally ineffective in dealing with the advanced stages of prostate cancer. (Kondo, et al., 2000). The aim of therapy is to prevent androgenic stimulation of the tumor. Efforts to remove the tumor and the surrounding tissue with androgen ablation are often combined with the blockade of the androgen receptor by various anti-androgens. Androgens are responsible for the regulation of growth and development of the prostate gland. The use of hormonal therapy will bring about initial success in treating prostate cancer but most tumors gradually progress to become androgen-independent. .
Novel modalities that are currently being studied include using antisense oligonucleotides to inhibit androgen receptors in prostatic carcinoma, genetically modifying lymphocytes with tumoricidal properties, suppressing the expression of telomerase in cancer cells with 2-5A-anti-telomerase RNA component, and using a combination of ovine adenovirus delivered PNP gene and fludarabine. Each of these new therapies shows substantial success in inducing apoptosis in prostate cancer cells or in reducing tumor volumes and growth.
